I’m a big proponent of the role of arterial aging in explaining dementia risk variance, in large part because it explains the large role that vascular-related risk factors have in promoting the likelihood of Alzheimer’s disease (AD). However, some data suggests that the burden of ischemic events and stroke cannot explain all of the vascular-related AD risk. Recently, Gutierrez et al. published a nice paper which suggests that non-atherosclerotic artery changes with age may explain some of this residual vascular-related risk of AD. In particular, they used 194 autopsied brains and found five arterial features which strongly correlated with aging, including decreased elastin and concentric intimal thickening. Importantly, these features also correlated with AD risk independently of age.
The authors propose that the arterial aging features are a consequence of mechanical blood flow damage that accumulates over the years. If it is true that the damage is mechanical, it suggests that it may be difficult to reverse with existing cellular and molecular anti-aging therapies. For those people who are interested in slowing down aging, the brain must be a top priority because it cannot be replaced even by highly advanced tissue engineering approaches to replace the other organs. Thus, this sort arterial damage needs to be addressed, but to the best of my knowledge it has not been, which is one of the many reasons that I expect that serious anti-aging therapies are much further out than are commonly speculated in the popular press.